1. Restriction and Constriction
Nick Tehrani, MD

2. Restrictive Cardiomyopathy
EVOLVED
As a bedside clinical diagnosis of constriction
confirmed by right heart catheterization findings of
constrictive physiology in patients who:
POROVED NOT TO HAVE ANY
PERICARDIAL DISEASE

3. Traditional Hemodynamic Criteria

4. Traditional Hemodynamic Criteria

5. Utilitity of: Traditional Hemodynamic Criteria
are of LIMITED Utility
Hurrell DG, Nishimura RA, Higano ST, Appelton CP, Danielson GK, Holmes DR, Tajik AJ. Value of dynamic respiratory changes in left and right ventricular pressures for the diagnosis of constrictive pericarditis. Circ. 1996; 93:

6. Restrictive Cardiomyopathy
Represents an extreme form of Diastolic Dysfunction:
Therefore, to understand Restriction, must start with a discussion of Diastole
Abnormal increase in Diastolic ventricular pressure impeding filling of the LV To NL EDV

7. Diastole: A historical view
Diastole as the passive interval between systolic events
Discovery of Frank-Starling mechanism:
LV-EDV, helps regulate the SV
Katz:
After MV opening, LV pressure continue to decline, despite LV volume incresase
Systlic failure as the only kind of failure recongized
LV-EDV => diastole more than just passive
LV as an active suction
pump in early diastole.

8. Diastolic Properties of the LV
End of IVRT
Active suction.
ATP req’d
To Re-uptake
Ca++

9. Quantitative assessent of the 4 phases of Diastole:
IVRT>100 ms
Earliest diastolic ab-normality.
Impaired LV relax.
Filling pressures=NL
Dz. progression:
Decreased LV compliance, and
Increased filling pressure
More specific quantitative approach to classification of Diastole
Late
diastolic filling
Diastasis
Early diastolic
filling
IVRT

10. Quantitative assessment of the 4 phases of Diastole:
IVRT
Early filling:
DT < ms
Interplay of Early and Late filling:
E:A ratios…….
If E at A> 20 cm/s => E/A unreliable
Tachycardia
PR prologgation
“A” wave duration…….
Utilized in relation to PV “a” wave duration.

11. E:A ratios, as a Function of Age
Impaired LV relaxation (IVRT )
Decreased LV Compliance
COPIED LATER
Restrictive
Pseudonormal

12. The three abnormal LV filling patterns
Comment on how do you know if it is pseudo, when no baseline patterns are available ala ECGs?
ANSWER: Compare with the PV flow pattern//// Cut out the last row, and save it and the next slide for a juxaposition of PV in RESTRICTION vs CONSTRICTION ala KLEIN’s paper.. COPIED LATER

13. Pathophysiologic Similarity of: Restriction and Constriction
Abnormal increase in ventricular
pressure
impeding filling of the LV To NL EDV
Constriction
Restriction
Myocardial
Disorder
Pericardial
Disorder

14. Anatomy Lt. Atrium is not completely intrapericardial
All other cardiac chambers are completely intrapericardial
Pulmonary Veins are completely intrathoracic

15. Effect of Inspiration Normal Pericardium:
Inspiratory decrease in intrathoracic pressure is uniformly transmitted to the lungs, PVs, LA, LV, RA, and RV

16. Effect of Inspiration Constrictive Pericarditis:
Thickened pericardium isolates the heart form transmission of intrathoracic pressure changes
Increased inspiratory capacitance of the Lungs PVs, and LA => PCWP decrease BUT
The decrease in intrathoracic pressure is not transmitted to the LV, RV, RA

17. Dissociation of Intrathoracic and Intracardiac Pressures
First demonstrated to be present in constrictive pericarditis using Doppler techniques in 1989, by Hatle in her landmark study.
Visiting at MAYO from Holland at the time.
Hatle LK, Appleton CP, Popp RL.
Differentiation of constrictive pericarditis
And restrictive cardiomyopathy by Doppler
Echocardiography. Circ. 1989;

18. Dissociation of Intrathoracic and Intracardiac Pressures
The inciting
Physiologic
Event.
Hatle LK, et. al.
Circ. 1989;

19. Ventricular Interdependence
Hatle LK, et. al.
Circ. 1989;
Ventricular Pressures
Are DISCORDANT
Insp
Expir

20. Traditional v.s. Dynamic Catheterization Hemodynamics
Why bother with Echo given
The great utility of Dynamic
Respiratory cath measurments?
These measurments are only
Possible using High-fidelity
Micromanometer systems
(not a common practice).
Dissociation of Intrathoracic
and Intracardiac Pressures

21. Effect of Inspiration: Constriction
Expir.
Insp.
Expir.
PCWP
PCWP
Inspir.
Expir.
PCWP
No proportionate decrease in LV diastolic pressure
Decreased transmitral gradient => Transmitral flow
RV SV
LV SV

22. Pathophysiologic Differences
Constriction
Restriction
Ab-Nl Myocardial compliance
Myocardial compliance is NL
No impedence to
Diastolic EARLY FILLING
Impedence to filling increases
throughout the diastole
Total cardiac volume is fixed by
the pericardium
Pericardium is compliant
Septum is non-compliant
Reduction of the proportion of
LV filling with atrial contraction:
=> Atrial enlargement
Atria are able to empty into the
Ventricles, though at higher Press.
Minimal Respiratory effect of
RV on the LV
Marked Respiratory effect of
LV on the RV

23. Specific Echocardiographic Criteria for Constriction/Restriction
Mitral E wave pattern
Pulmonary Vein pattern
Hepatic Vein pattern

24. Mitral E wave Criteria for Constriction
Decrease in of 25% in Mitral “E” velocity on inspiration.

25. In RESTRICTION:
There is no respiratory variation of Mitral inflow

26. Specific Echocardiographic Criteria for Constriction/Restriction
Mitral E wave pattern
Pulmonary Vein pattern

27. Normal PV Flow-TTE PSV1- LA relaxation and pressure decrease.
PSV2- Interaction of RV-SV, w/ LA pressure and compliance.
PVa duration- Interplay of multiple factors
Now go back to the previous Slide and drive home the point regarding the Dx of Pseudo
Utilized in relation to Mitral “A” wave duration.

28. Three abnormal PV filling patterns in Restriction
Seen this slide once before

29. E:A ratios, as a function of Age
Impaired LV relaxation (IVRT )
Decreased LV Compliance
Seen this slide once before
Pseudonormal
Restrictive

30. Relation of Mitral “A” wave to Pulmonary Venous “a” wave duration
Normal Physiology
With LA contraction
Forward flow Volume and Duration
Exceeds
Backward flow into the PV

31. Relation of Mitral “A” wave to PV “a” wave duration
Restrictive Physiology:
PV-a Velocity > 35 cm/s OR
PV-a duration, 30 ms longer than Mitral “A” wave duration.
200 ms
Above findings suggestive of elevated LV end diastolic pressure
121 ms

32. PVs are best assessed using TEE
PV interrogation using TTE is often
techniaclly limited.
PVs are best assessed using TEE

33. Normal PV Flow-TEE NO Variation from Inspiation to Expiration
Rt. Upper PV
NO Variation from Inspiation to Expiration
Kline-1937
LV inflow

34. PV Dopplar Patterns in Restriction-TEE
Lt. Upper PV
PV flow is not respirophasic
Systolic/Diastolic velocity is
markedly down in both inspiration
and expiration
Kline 1939, 1993JACC
LV Inflow
LV inflow Peak-E velocity is
not respirophasic

35. PV Dopplar Patterns in Costriction-TEE
Lt. Upper PV
PV flow IS Respirophasic:
25% variation of both the Systolic and Diastolic components
Systolic/Diastolic
Ratio higher than for restriction
(0.7 v.s. 0.4)
LV Inflow
LV inflow Peak-E:
17% respiratory variation
(v.s. none for restriction)

36. Specific Echocardiographic Criteria for Constriction/Restriction
Mitral E wave pattern
Pulmonary Vein pattern
Hepatic Vein pattern

37. Respiratory Cycle :Hepatic Vein Flow
IVC
Inspiration
Expiration

38. Hepatic Vein Dopplar: Normal
Systolic and diastolic forward flow
S-vel. > D-vel.
Diastolic flow reversal:
Expir.>>Insp.

39. Hepatic Vein Dopplar: Constriction
Diastolic flow reversal is
augmented in expiration.
DFRexp.>25% forward
diastolic velocity

40. Hepatic Vein Dopplar: Restriction
Forward flow primarily in
Diastole.
Inspiration increases both
>systolic, and
>Diastolic
Flow reversals.

41. Hepatic Vein Dopplar: Compilation
Nasser S Tehrani:
These pts not respond as well to surgery
Hepatic Vein Dopplar: Compilation
Mixed physiology
(restriction/constriction)
Diastolic flow reversal
during both Ispiration
and expiration

42. Constriction Doppler
Inspiration
Expiration

43. Animation

44. Animation

45. Pitfalls and Caveats
Subgroup of patients with constriction who do not exhibit respiratory changes
COPD
Such Pts comprised 12% of Pts in a series of ???, reported by Oh JACC 1994;23:

46. Constriction: Non-respirophasic
Oh et. al. Circ. 1997;95:
12 Pts. W/ confirmed constriction, but without the classic findings
Etiology of Non-respirophasic pattern
Mixed Restriction and Constriction
Marked increase in Preload
Oh Circ 1997; 95:
Deduced post
Stripping, as Sx
Not improve
Preload reduction to
unmask the respiratory
variation

47. Constriction: Non-respirophasic
Nasser S Tehrani:Wide STD.Deviation, But may be diagnostic for a ginven pt.
Constriction: Non-respirophasic
Supine
Supine
Sitting
Oh 180-A
Insp.
Expir.
Insp.
Expir.
Sitting

48. Effect of changing loading conditions w/ VALSALVA in RESTRICTION
A to a lesser degree

49. Pitfalls and Caveats
Subgroup of patients with constriction who do not exhibit respiratory changes
COPD

50. COPD v.s. Constriction 100% change in E Velocity
Individual Mitral flow velocity profiles are not restrictive as LV filling pressure is not increased.

51. COPD v.s. Constriction COPD: Greater than NL Increased SVC Flow COPD
decrease in intrathroracic
pressure is generated with
inspiration =>
Increased SVC Flow
Const.
Constriction: Minimal change in SVC velocities with inspiration.

52. Tissue Dopplar PW Analysis of Mitral Annular Motion
Physiologic Premise:
Assessment of VELOCITY of LV
-Contraction, and
-Relaxation

53. How to: TDI function of the machine is activated
Gain is lowered to approx. Zero
Wall filters are minimized to display lower velocities (annular velocity < 20 cm/s)
Sweep at 100 or 200 mm/sec
Apical 4 chamber minimizes the translational and rotational components of LV Contraction.
THEREFORE, ONLY AXIAL COMPONENT OF VELOCITY IS INTACT

54. Tissue Dopplar: Restriction and Constriction
Mitral inflow E wave is elevated in both
Annular E wave
Restriction, peak E-wave < 8 cm/sec
Constriction, Peak E-wave > 8 cm/sec
The above is Premised on the assumption that:
Annular E wave is preload independent.
Both Pro- and Con- studies regarding this premise exist.

55. Constriction v.s. Restriction
Dx has important therapeutic implications
Clinical Presentaion similar: RHF
Historical etiologies helpful, but not diagnostic
A thick pericardium is not necessarily constrictive
A restrictive process may constrict
Echo and Hemodynamic features may overlap

56. Restrictive Cardiomyopathy
Broad categories of diseases involved:

57. Etiologies of Constriction
Infectious: Post-viral, TB, Purulent
Traumatic:Post CABG, Pacer, Sternal trauma
Post XRT
Chronic inflammatory Dz: RA, SLE
Uremia
Neoplasia

58. The End